Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Allergic diseases are one of the most common chronic non-infectious diseases in childhood，primarily resulting from genetic and environmental interactions.Evidence suggests that maternal exposure to risk factors during pregnancy can impact the fetus through the placenta，leading to immune dysregulation，disruptions in gut microbiota composition，and ultimately contributing to the development of allergic diseases in children.Therefore，maternal pregnancy represents a critical period for preventing allergic diseases in children.This article provides an overview of research advancements regarding the influence of environmental risk factors during pregnancy on allergic diseases in children，focusing on aspects such as maternal diet，medication usage，maternal illnesses during pregnancy，and allergen exposure，so as to provide new strategies for preventing childhood allergic diseases.

Objective:To explore effect of rubusoside(RS) on myocardial injury in gestational diabetes mellitus(GDM) rats and its mechanism.Methods:Pregnant SD rats were divided into control, GDM model, insulin treatment(INS), RS, endoplasmic reticulum stress inhibitor 4-phenylbutyric acid(4-PBA), and RS+ endoplasmic reticulum stress inducer thapsigargin(THA) groups. Glycolipid metabolism, cardiac function, serum LDH, cTnI, and CK-MB levels, myocardial tissue morphology, SOD, GSH, MDA, Fe 2+ content were assessed. ROS levels were assessed using DHE staining, and iron ion deposition was evaluated via Prussian blue staining. The expression of endoplasmic reticulum stress and ferroptosis related proteins in myocardial tissue after intervention was analyzed through Western blot and immunohistochemistry. Results:Compared with control rats, GDM model rats showed increased body weight, FBG, TC, TG, abnormal cardiac function, significant myocardial damage, elevated serum LDH, cTnI, CK-MB, reduced SOD and GSH, increased MDA, Fe 2+, ROS, and iron ions, along with altered protein expression indicating endoplasmic reticulum stress and ferroptosis. RS and 4-PBA mitigated these changes, reducing myocardial injury. THA reversed RS′s protective effects via the endoplasmic reticulum stress-ferroptosis pathway. Conclusion:RS improves glycolipid metabolism and alleviates myocardial injury in GDM rats by inhibiting endoplasmic reticulum stress and reducing ferroptosis.

Objective:To observe the effects of muscle regions of meridians needling method combined with auricular point sticking on pain and lumbar range of motion in patients with chronic nonspecific low back pain. Methods:A total of 100 patients with chronic nonspecific low back pain were randomly divided into a control group and an observation group,with 50 patients in each group.Both groups received auricular point sticking treatment,while the control group received additional conventional acupuncture treatment,and the observation group received additional muscle regions of meridians needling method.The total effective rate of the two groups was compared after 4 weeks of treatment.Before treatment and after 1 week and 4 weeks of treatment,the visual analog scale(VAS)score was used to assess the degree of low back pain,and the modified-modified Schober(MMS)score was used to evaluate the lumbar range of motion. Results:There was statistical significance in comparing the total effective rate between the two groups(P<0.01).During the treatment process,as the number of treatments increased,the VAS score gradually decreased,and the MMS score gradually increased in both groups.After 1 week and 4 weeks of treatment,the VAS score in the observation group was lower than that in the control group(P<0.01),and the MMS score in the observation group was higher than that in the control group(P<0.01).During the treatment period,no serious adverse reactions occurred in either group. Conclusion:Based on auricular point sticking treatment,muscle regions of meridians needling method is more effective than conventional acupuncture in treating chronic nonspecific low back pain since it is able to significantly reduce the pain and improve the lumbar range of motion.

This study aimed to observe the protective effect of momordicine I, a triterpenoid compound extracted from momordica charantia L., on isoproterenol (ISO)-induced hypertrophy in rat H9c2 cardiomyocytes and investigate its potential mechanism. Treatment with 10 μM ISO induced cardiomyocyte hypertrophy as evidenced by increased cell surface area and protein content as well as pronounced upregulation of fetal genes including atrial natriuretic peptide, β-myosin heavy chain, and α-skeletal actin; however, those responses were markedly attenuated by treatment with 12.5 μg/ml momordicine I. Transcriptome experiment results showed that there were 381 and 447 differentially expressed genes expressed in comparisons of model/control and momordicine I intervention/model, respectively. GO enrichment analysis suggested that the anti-cardiomyocyte hypertrophic effect of momordicine I may be mainly associated with the regulation of metabolic processes. Based on our transcriptome experiment results as well as literature reports, we selected glycerophospholipid metabolizing enzymes group VI phospholipase A 2 (PLA2G6) and diacylglycerol kinase ζ (DGK-ζ) as targets to further explore the potential mechanism through which momordicine I inhibited ISO-induced cardiomyocyte hypertrophy.Our results demonstrated that momordicine I inhibited ISO-induced upregulations of mRNA levels and protein expressions of PLA2G6 and DGK-ζ. Collectively, momordicine I alleviated ISO-induced cardiomyocyte hypertrophy, which may be related to its inhibition of the expression of glycerophospholipid metabolizing enzymes PLA2G6 and DGK-ζ.

Objective:To construct a scientifically standardized and promotable pneumonia prevention and nursing plan for acute stroke patients to guide clinical nursing practice.Methods:According to the evidence-based retrieval strategy, we systematically searched the domestic and foreign clinical decision support system, guideline networks, professional association websites and relevant databases. All databases were searched from January 2012 to November 2022. A preliminary pneumonia prevention and nursing plan for acute stroke patients was formulated after literature quality evaluation, evidence extraction, evidence integration and evaluation. The plan was further revised and improved through three rounds of Delphi expert consultation.Results:In the three rounds of expert consultation, the enthusiasm of experts was 100.0%, 100.0%, 83.3%, the authority coefficient of experts were 0.967, 0.967, 0.937, the coefficient of variation were 0.048 to 0.363, 0 to 0.177, 0 to 0.144, and the Kendal harmony coefficient were 0.221, 0.139, 0.339 ( P<0.001) . The final nursing plan included 8 modules, including pneumonia risk prediction, general nursing, swallowing and dietary management, airway management, oral management, position and exercise, condition observation, and health education, with a total of 30 items. Conclusions:The evidence and Delphi method based pneumonia prevention and nursing plan for acute stroke patients is scientific, reliable and applicable, which can provide a basis for nursing practice.

Objective:To explore independent predictors of postoperative delirium in elderly patients by PRe-Operative Prediction of postoperative DElirium by appropriate SCreening (PROPDESC) and Mayo Delirium Prediction (MDP) , and analyze the predictive power of the two models.Methods:This study was a prospective Cohort study. Using the convenient sampling method, a total of 636 elderly surgical patients admitted to the Orthopedics, Gastroenterology, Cardiothoracic and Oncology Departments of Shantou Central Hospital from May to August 2022 were selected as the research objects. PROPDESC and MDP were used to predict postoperative delirium in elderly patients. The area under the receiver operating characteristic ( AUC) and diagnostic characteristics of the two predictive models were compared, and the single factor analysis and Logistic regression analysis were performed on 19 predictive factors of the two models to determine the independent influencing factors of postoperative delirium. Results:The AUC for external verification of the PROPDESC and MDP were 0.87 (95% CI: 0.84-0.90) and 0.89 (95% CI: 0.86-0.92) , respectively. The sensitivity of 71.79% and 80.34%, and specificity of 85.16% and 81.12%, respectively. Logistic regression analysis showed that emergency admission, age, sentence repetition and sequence subtraction in Montreal Cognitive Assessment (MoCA) were independent influencing factors for postoperative delirium ( P<0.05) . Conclusions:The predictive ability of PROPDESC and MDP models to predict postoperative delirium in elderly patients is satisfactory. On this basis, delirium risk assessment tools suitable for different surgical elderly populations in China can be constructed.